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Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
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The gastric glands contain parietal cells that secrete hydrochloric acid (HCl) for digestion. The cells secrete HCl because it is highly corrosive and essential for breaking down food. To achieve this, they secrete hydrogen and chloride ions into the lumen of the gastric glands, which combine to form HCl.
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STING activation promotes intestinal mucin secretion in IBD.

Yuchen Yang1, Tjasso Blokzijl1, Antonio Miguel da Costa de Pina1

  • 1Department of Gastroenterology and Hepatology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.

Biochimica Et Biophysica Acta. Molecular Basis of Disease
|March 24, 2026
PubMed
Summary

STING pathway activation in inflammatory bowel disease (IBD) leads to increased mucus release, explaining goblet cell depletion. This study investigated STING

Keywords:
Goblet cellsHuman intestinal organoids.Inflammatory bowel diseasesMucincGAS-STING

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Area of Science:

  • Gastroenterology
  • Immunology
  • Cell Biology

Background:

  • Goblet cells and mucus protect the intestinal lining.
  • Inflammatory bowel diseases (IBD) are linked to goblet cell loss and mucus layer disruption.
  • The cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway's role in goblet cell depletion is complex, with both deficiency and overactivation causing issues.

Purpose of the Study:

  • To investigate the role of the cGAS-STING pathway in regulating goblet cell mucus production in IBD patients.
  • To analyze STING pathway activation and MUC2 expression in human colonic organoids (HCO).

Main Methods:

  • Analyzed MUC and cGAS-STING gene expression in IBD patient mucosa (n=821) and controls.
  • Performed MUC2 and STING pathway immunohistochemistry.
  • Treated human colonic organoids (HCO) with STING agonist (diABZI) and antagonist (H151).
  • Assessed STING activation and MUC2 regulation using qPCR, Western blotting, and immunofluorescence microscopy.

Main Results:

  • Inflamed IBD mucosa showed increased MUC and cGAS-STING pathway gene expression.
  • Reduced mucus-filled goblet cells were observed in inflamed IBD mucosa, despite increased immature MUC2 and activated STING.
  • STING activation in HCO led to increased mature MUC2 accumulation and reduced mucus-filled goblet cells.
  • STING antagonism did not decrease mucus-filled goblet cells in HCO.

Conclusions:

  • STING pathway activation promotes excessive mucus release in inflamed IBD epithelium.
  • This enhanced mucus release provides a mechanistic explanation for the observed histological depletion of goblet cells in IBD.